Necrotizing Myositis: A Rare Necrotizing Soft Tissue Infection Involving Muscle

A Rare Necrotizing Soft Tissue Infection Involving Muscle

Harika Boinpally, MD; Raelina S. Howell, MD; Bebu Ram, MD; Virginia Donovan, MD; Michael Castellano, MD; Jon S. Woods, MD; Scott Gorenstein, MD, FACEP


Wounds. 2018;30(12):E116-E120. 

In This Article


Necrotizing soft tissue infections are an aggressive group of infections requiring immediate surgical attention. Although NSTIs are known for their fulminant disease course, patients can present with vague, nonspecific symptoms before rapidly progressing to life-threatening septic infection, thereby requiring a high index of suspicion. Necrotizing myositis is a rarely encountered NSTI involving the skeletal muscle. Various pathogens have been identified in NM cases and the organisms commonly isolated are group A beta-hemolytic Streptococcus(GABHS), C perfringens, and C septicum. To the best of the authors' knowledge, this report is the first case of NM caused by C clostridioforme and S intermedius.

Patients with a NSTI may have nonspecific clinical findings with or without pain, swelling, and redness of the affected area. Worsening pain out of proportion to physical exam, edema, and inability to bear weight may occur as the disease progresses. Initially, the skin overlying the affected area may appear normal but become discolored with bullae, blisters, vesicles, or petechiae as the infection progresses. Systemic findings such as fever, tachycardia, hypotension, and shock may be present. Although NSTI is a clinical diagnosis, the aforementioned signs and symptoms occur in only 10% to 40% of patients.[1] Laboratory findings are nonspecific and often show elevated WBC, Cr, lactate, Cr kinase, and coagulopathy.[1]

Sensitivities of CT and MRI in detecting NSTI are 80% to 85% and 90% to 100%, respectively.[2] Although MRI is a more sensitive imaging modality, it could potentially delay treatment, making CT a diagnostically convenient early imaging option.[2] Computed tomography can demonstrate air within the fascia, thickening and edema of the involved muscle/fascia, fluid tracking, lymphadenopathy, and deep tissue collections,[2] whereas MRI can demonstrate subcutaneous thickening with fluid collection and inflammatory response to the muscle.[3] As NSTIs are clinically diagnosed, imaging results should not delay surgery in the presence of strong clinical suspicion.[2]

Management of NSTIs include prompt diagnosis and early surgical intervention. Surgery within 24 hours significantly increases survival.[4] Surgical-site inspection within 24 hours following initial debridement, serial debridement every 48 to 72 hours, and removal of necrotic tissue are important management steps.[4] Although the benefit of adjunctive HBOT remains controversial, the results of recent, small, retrospective studies have supported the use of HBOT for patients with NSTIs.[5,6]

Histopathology of tissue obtained during surgery is important to confirm the diagnosis and differentiate a NSTI from idiopathic inflammatory myopathy (eg, polymyositis, dermatomyositis, inclusion body myositis). Histologically, NM demonstrates interstitial inflammation with muscle fiber necrosis[7] and lacks the mononuclear inflammatory cell infiltrates seen in idiopathic inflammatory myopathy (Figure 4A). Tissue and culture specimens obtained during surgery also are important for organism identification and subsequent, targeted antibiotic treatment. Organisms identified in this case report were S intermedius, C clostridioforme, and Peptostreptococcus. Macnicol[8] described a case of myositis caused by S milleri in 1977, but the exact species involved was not reported. S intermedius, a normal flora of oral cavity and gastrointestinal tract, can cause systemic infections and abscesses[9] and, when isolated, is considered a true pathogen.[10] It has many virulent strains, of which strain B-196 is associated with pyomyositis, osteomyelitis, sepsis, arthritis, and bronchopulmonary infections.[11,12]Osteomyelitic changes seen on the present patient's CT and cystogram can be attributed to the purulent infection eroding the adjacent bone and also the osteomyelitic properties of virulent B-196 strain of S intermedius. S intermedius is known to produce a cytolytic toxin called intermedilysin, an important virulent factor for deep abscess.[13] Hyaluronidase and deoxyribonuclease are other potent enzymes produced by S intermedius that aid in spreading infections through tissues by causing liquefaction and pus formation.[14]

C clostridioforme is an anaerobic, gram-positive bacillus that stains gram negative. It is part of normal colonic microflora.[15] It is known to cause severe bacteremia, necrotizing fasciitis, pelvic-intraabdominal abscesses, and postoperative wound infections, especially in abdominal, perineal, and perianal regions.[16] As in the present patient, cancer was an underlying condition in previously reported cases.[16]

Peptostreptococcus is an anaerobic, gram-positive bacterium found in the normal flora of mucocutaneous surfaces. It is commonly isolated from infections such as deep-organ abscesses. Three cases of Peptostreptococcus were reported as a cause of NM in the year 1972.[17] Research has demonstrated the concept of microbial synergy (ie, promoting and enhancing the growth of other organisms) as an important contributing virulence factor for developing deep infections, thereby indicating that the presence of Peptostreptococcus along with other virulent organisms (S intermedius and C clostridioforme as in this case) has the potential to accelerate sepsis and increase mortality.[18]